C H A P T E R 2 8
Common
Neurologic Disorders
LEARNING OBJECTIVES
Upon completion of this chapter,
the reader will be able to:
1. Discuss the cerebral vascular
circulation.
2. Outline the sensory and muscular
spinal nerves.
3. Summarize the pathology of com-
mon neurologic disorders.
4. Identify evidence-based interven-
tions for common neurologic
disorders.
5. List optimal outcomes that may be
achieved through evidence-based
management of common neuro-
logic disorders.
Krista M. Garner
euroscience nursing has emerged as one of the fastest-growing areas of specialty
N practice (Hickey, 2003). Advancements in both neuroscience research and clin-
ical practice are providing new and exciting roles for registered and advanced practice
nurses. Healthcare trends have encouraged the specialty practice of neurocritical care
collaborative teams based on favorable patient and financial outcome results in cur-
rent literature (Suarez et al., 2004; Varelas et al., 2004). With the assumption of new
roles in practice come greater responsibilities and accountability for providing the
highest level of care for the neurologic patient. To achieve these goals, the neuroscience
critical care nurse must have a strong neuroscience knowledge base from which to
grow in complexity, as the ever-changing evidence-based research drives the practice
trends to higher levels of reasoning and decision making.
This chapter begins by providing a brief overview covering spinal nerve roots and
cerebrovascular circulation. Understanding the complex anatomy of the cerebrovas-
culature is essential when caring for the critically ill neurologic patient. Complications
involved with the blood supply of the brain are generally most prevalent in neurocrit-
ical care, accounting for a large percentage of poor neurologic outcomes.
Cerebral circulation is the responsibility of two pairs of arteries: the two internal
carotid arteries, accounting for anterior circulation, and the two vertebral arteries, ac-
counting for posterior circulation. Each area of circulation includes distal branches as
well as communicating penetrators responsible for a constant and well-networked
blood supply. Table 28-1 and Table 28-2 describe the major cerebral branches and the
areas they supply.
The spinal cord is an elongated mass of nerve tissue from which 31 pairs of spinal
nerves exit: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each spinal
nerve has a dorsal root by which afferent impulses enter the cord and a ventral root by
which efferent impulses leave. The dorsal roots convey sensory input from specific
areas of the body known as dermatomes. The ventral roots convey motor impulses,
known as myotomes, from the spinal cord to the body (Table 28-3).
MANAGING ELEVATED INTRACRANIAL PRESSURE
Elevated intracranial pressure (ICP) is one of the major deteriorating factors in patients
with intracerebral lesions (Forster & Engelhard, 2004). Because the cranium is rigid and
 376 CHAPTER 28 Common Neurologic Disorders

TABLE 28-1 Major Internal Carotid Arterial Branches

Artery Area Supplied

Ophthalmic Orbits and optic nerves

Posterior communicating (Pcom)
Anterior choroidal
Anterior cerebral (ACA)
Recurrent artery of Heubner
Middle cerebral (MCA)
Lenticulostriate (from MCA)
Anterior communicating (Acom)
Connects the carotid circulation with the vertebrobasilar circulation
Part of choroid plexuses of lateral ventricles; hippocampal formation; portions of globus
pallidus; part of internal capsule; part of amygdaloid nucleus; part of caudate nucleus; part of
putamen
Medial surfaces of frontal and parietal lobes; part of cingulated gyrus and “leg area” of
precentral gyrus
Special branch of ACA; penetrates the anterior perforated substances to supply part of the
basal ganglia and genu of internal capsule (also called medial striate artery)
Entire lateral surfaces of the hemisphere except for the occipital pole and the inferolateral
surface of the hemisphere (supplied by posterior cerebral artery)
Part of basal ganglia and internal capsule
Connects the two ACAs

Source: Reprinted with permission from Emory University.

noncompliant, any increase in cerebral volume will, in turn, el-
evate cranial pressure (Figure 28-1). The major pathophysio-
logic problems associated with increased ICP are ischemia and
herniation (Josephson, 2004).
The normal range of ICP is 0 to 15 cm H2O. Elevations be-
yond these levels can rapidly lead to brain damage. Cerebral
perfusion pressure (CPP) is mean arterial pressure minus ICP.
Global ischemic injury results from a critical reduction of CPP,
and thus of cerebral blood flow (CBF). Mechanical compres-
sion and herniation of brain tissue—the second mechanism of
injury—occurs with space-occupying mass lesions and com-
partment syndrome of brain contents (Josephson, 2004).

TABLE 28-2 Major Vertebral Arterial Branches and the Cerebral Areas They Innervate
Artery Area Supplied

Vertebral Branches
Anterior spinal
Posterior spinal
Posterior inferior cerebellar (PICA)
Basilar Artery Branches
Posterior cerebral (PCA)
Posterior choroidals (from PCA)
Medial posterior choroidal
Lateral posterior choroidal
Anterior inferior cerebellar artery (AICA)
Superior cerebellar artery (SCA)
Pontine
Anterior two-thirds of spinal cord
Posterior one-third of spinal cord
Undersurface of the cerebellum, medulla, and choroid plexuses of fourth ventricle
Occipital lobes, medial and inferior surfaces of the temporal lobes, midbrain, and choroid
plexuses of third and lateral ventricle
Tectum, choroid plexus of third ventricle, and superior and medial surfaces of the
thalamus
Penetrates the choroidal fissures and anastomosing with branches of the anterior
choroidal arteries
Undersurface of the cerebellum and lateral surface of the pons
Upper surface of the cerebellum and midbrain
Pons

Source: Reprinted with permission from Emory University.

 Common Neurologic Disorders and Evidence-based Interventions 377

saline. Both are extremely effec-

TABLE 28-3 Sensory Nerve Roots (Dermatome) and Motor Nerve Roots (Myotomes) tive initial treatment modalities
and the Areas They Innervate
when bolused for the reduction
Dermatome Muscles of ICP.
Spinal Nerves (Sensory Nerve Roots) (Motor Nerve Roots)
Anesthetic and Paralytic
C-2 Back of head Neck
Agents
C-3 Neck Neck
C-4 Neck and upper shoulder Neck, diaphragm Sedation using hypnotic, nar-
C-5 Lateral aspect of shoulder Neck, diaphragm
cotic, and paralytic agents is
performed to reduce stress and
C-6 Thumb; radial aspect of arm Diaphragm, shoulder, elbow
to control ICP (Forster &
C-7 Middle finger; middle palm; back Forward thrust of shoulder
of hand
Engelhard, 2004). The drugs are
chosen to achieve the effects of
C-8 Ring and little finger; ulnar Adduction/extension of arm,
forearm wrist decreased cerebral metabolic rate
T-1, T-2 Inner aspect of the arm; shoulder Control of thoracic, abdominal,
and reduced CBF and cerebral
blade and back muscles (T-1 to T-12) blood volume (CBV).
T-4 Nipple line
T-7 Lower costal margin Ventilation
T-10 Umbilical region The respiratory alkalosis caused
T-12, L-1 Groin region by induced mechanical hyper-
L-2 Anterior thigh and upper Flexion of hip ventilation can quickly and ef-
buttocks fectively lower ICP by causing
L-3, L-4 Anterior knee and lower leg Extension of leg cerebral vasoconstriction and re-
L-5 Dorsum of foot; great toe Flexion of foot duced CBV (Josephson, 2004).
S-1, S-2, S-3 Foot, toes, medial thigh Perineal area and sphincters Hyperventilation is conducted to
S-4, S-5 Genitals area
get the PCO2 at a level between
30 and 35 mm Hg. Even though
it is an effective acute inter-
Sources: Hickey, 2003; Wijdicks, 2003.
vention for increased ICP, pro-
longed hyperventilation should
be avoided due to the increased
Following is a list of the most current options in the literature risk of cerebral ischemia with excessive vasoconstriction
today for the treatment of increased ICP. Chapter 27 discusses (Steiner et al., 2005).
ICP monitoring in more detail. Other treatment modalities for the treatment of increased
ICP drawing interest in the literature include induced hypother-
Head and Body Position mia (Commichau, Scarmeas, & Mayer, 2003; Shiozaki et al.,
Because cerebral venous outflow is obstructed, ICP increases 2003) and early surgical decompression via craniectomy
when the head is in a non-neutral position (Forster & (Albanese, Leone, & Alliez, 2003; Cho, Chen, & Lee, 2003).
Engelhard, 2004). Durward, Amacher, and DelMaestro (1983)
have shown that elevation of the head to 15 to 30 degrees pro- COMMON NEUROLOGIC DISORDERS AND
duces a consistent reduction of ICP. EVIDENCE-BASED INTERVENTIONS
Neurologic dysfunction can be a result of a multitude of dif-
Osmotic Agents ferential diagnoses and, when severe enough, will require in-
In osmotic drug therapy, an osmotic pressure difference is in- tensive critical care with specific, timely, and well-organized
duced between the blood and the brain, thereby causing extrac- nursing care. Critical care management is not always standard
tion of water from the cerebrum into the intravascular space procedure, but rather varies depending on the case and the
(Josephson, 2004). Two osmotic drugs are most commonly patient. Thus it allows room for interpretation and interven-
used in this manner: mannitol (Osmitrol®) and hypertonic tion based on research, experience, and advanced knowledge.
 378 CHAPTER 28 Common Neurologic Disorders

FIGURE 28-1 ICP Waveform Pulsatility—Cerebral Hyperemia Increased Blood Volume Hemorrhagic Stroke
Raised ICP There are two types of hemor-
rhagic stroke: intracranial hem-
orrhage (ICH), which occurs
with bleeding into the brain tis-
sue, and subarachnoid hemor-
rhage (SAH), which occurs with
bleeding into the subarachnoid
space beneath the arachnoid
mater of the meninges. Clinically,
ICH provokes the same effect on
the brain as space-occupying le-
sions and is often related to con-
tusions from traumatic brain
injury. If unable to be surgically
evacuated, ICH is often associ-
ated with a poor outcome and in-
creased mortality, secondary to
increased ICP with potential for
brain herniation.
SAH is most often the result
Source: Reprinted with permission from Marshall & Mayer (1997) On Call: Neurology (p. 159).
of a ruptured cerebral aneurysm.
Typically, the patient presents
acutely, without warning, with
The following are some of the most common neurologic diag- what is described as “the worst headache” of the patient’s life.
noses and current evidence-based interventions for care rele- After aneurysmal rupture, 10% of patients die suddenly, be-
vant to the intensive care unit (ICU) nurse. fore ever receiving medical attention. Of the patients who reach
the emergency department or neuroscience ICU, 20% to 30%
Cerebrovascular Complications arrive comatose and die within three months (Wijdicks, 2003).
Hemorrhagic and ischemic stroke are two of the principal The primary step in the management of SAH is aneurys-
complications of the cerebral vasculature. Of those patients mal repair, either by surgically clipping the neck of the
suffering from strokes in the United States each year, approx- aneurysm or by occluding the sac by endovascular coiling tech-
imately 80% to 85% experience ischemic stroke, while 15% to nique. Whether the aneurysm is repaired or not, intensive neu-
20% undergo hemorrhagic stroke. rologic monitoring is required due to the high prevalence of
secondary complications imposed by the initial traumatic
Ischemic Stroke event (Box 28-2).
An ischemic stroke results from the acute interruption of SAH is graded on a scale from grade I (asymptomatic or
blood flow to a volume of brain tissue supplied by an artery minimal headache) to grade V (presenting in a deep coma).
(Singh, 2004). It is, therefore, a central cause of brain damage The Hunt and Hess grading scale was developed in 1958 to
in neurologic patients, making prevention a primary mission classify cerebral aneurysms. Several complications are asso-
for the medical community. The term “time is brain” rings ciated with an SAH: rebleeding, cerebral vasospasm, and vol-
true for the intensive care patient, because prolonged reduc- ume and osmolar disturbances, such as hypernatremia.
tion or absence of blood flow to a certain area of the brain Management of patients with an SAH includes blood pres-
results in irreversible neuronal injury. Goals for managing the sure control and aneurysm precautions: a quiet, dark room
patient with acute ischemic stroke are twofold: (1) enhance- with minimal stimulation; elevation of the head of the bed to
ment of CBF and (2) neuroprotection, with the aim to reduce 30 degrees; blood pressure control; and pain control for
the intrinsic vulnerability of brain tissue to ischemia (Singh, headache. To prevent vasospasms, triple-H therapy is uti-
2004) (Box 28-1). lized: hypervolemia, hemodilution, and hypertensive ther-
 Common Neurologic Disorders and Evidence-based Interventions 379

Box 28-1
Treatment Interventions for Managing the Patient with
Ischemic Stroke
Thrombolytic Therapy (tPA)
• Supported through research
• Reopen occluded vessels with IV medications such as tPA
• Narrow time window (3–6 hours)
• Strict inclusion/exclusion criteria
Data from National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group, 1995.

Anticoagulant/Antiplatelet Therapy
• Controversial
• Prevents progression or reoccurrence of stroke using IV or low-molecular-weight heparin
Data from Caplan, 2004.
Management of Increased ICP and Cerebral Edema
• Mannitol, 3% saline
• Hyperventilation
• Sedation
• Decompressive surgery
Data from National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group, 1995; Caplan, 2004.

Blood Pressure Management

• Controversial
• Some trials suggest lowering BP can have adverse effects
• Lowering BP usually deferred unless end-organ damage is present or MAP 130 mm Hg or SBP  220 mm Hg
Data from Ahmed, Nasman, & Wahlgren, 2000; Adams, Brott, & Cromwell, 1994.

Strict Glycemic Control

• Associated with improved outcome in stroke patients
• Goal is to maintain blood glucose 80–110 mg/dL with IV insulin
Data from Juvela, Siironen, & Kuhmonen, 2005; Paolino & Garner, 2005.

Fever Control/Induced Hypothermia

• Shown to improve cerebral ischemic injury especially in cardiac arrest patients
• Neuroprotective strategy
Sources: Commichau, Scarmeas, & Mayer, 2003.

apy. The first goal of therapy is to keep the patient’s central ve-
nous pressure reading at 10 to 12 mm Hg and pulmonary ar-
tery occlusive pressure at 15 to 18 mm Hg through the use of
volume expanders such as colloids or crystalloids. The second
goal is to maintain a patient’s hematocrit between 33% and
38% by administering blood transfusions or performing phle-
botomy treatment on polycythemic patients. The third goal
with triple-H therapy is to manage hypertension by maintain-
ing a systolic blood pressure between 110 and 160 mm Hg.
Status Epilepticus
Status epilepticus (SE), or continuous seizure activity, is a med-
ical emergency that requires rapid and vigorous treatment to
prevent neuronal damage and systemic complications.
 380 CHAPTER 28 Common Neurologic Disorders

Box 28-2
Secondary Complications as a Result of Aneurysmal SAH
Rebleeding of Unrepaired Aneurysm
• Highest percentage within the first 24 hours of the initial bleed
• 30% risk in the first month
Data from Ohkuma,Tsurutani, & Suzuki, 2001.

Acute Hydrocephalus
• Occurs as a result of blood obstructing the reabsorption process from the subarachnoid space
• Many times relieved with the placement of a ventricular drain
• Dangerous elevation in ICP if CSF is not diverted via external shunting

Respiratory Failure
• Mainly a product of decreased level of consciousness with an inability to protect the airway
• Requires intubation through acute phase of illness

Neurogenic Cardiac Stunning

• Transient ischemic injury to the myocardium
• Produces inefficient cardiac function

Vasospasm
• Delayed cerebral ischemia occurring in 70% of patients with aneurysmal SAH
• May lead to symptomatic brain ischemia or infarct in 36% of all patients
• Classically occurs during post initial bleed days 4–15
• Treatment options include: triple-H therapy (hemodilution, hypertension, and hypervolemia), cerebral angiogram
with angioplasty, and systemic or intra-arterial calcium channel blockers
Sources: Liu-Deryke & Rhoney, 2006; Sen & Albon, 2003.

Management of the patient with SE should focus on termina-
tion of seizures, prevention of seizure recurrence once status
is controlled, management of precipitating causes of SE, and
management of complications (Chapman, Smith, & Hirsch,
2001). Along with clinical correlation, electroencephalographic
confirmation of SE should be accomplished as early as possi-
ble so that treatment strategies (Box 28-3) can quickly be im-
plemented. Cerebral metabolic decompensation occurs after
approximately 30 minutes of uncontrolled convulsive activity
(Chapman et al., 2001).
Four types of seizures may occur: focal motor, general-
ized tonic-clonic, complex partial, and nonconvulsive status. A
focal motor seizure involves the face or limb and often moves
from distal to proximal. A generalized tonic-clonic seizure re-
sults in a convulsion with tongue biting followed by a postic-
tal period of altered sensorium and urinary loss. A complex
partial seizure manifests with an aura that can be followed by
a tonic-clonic seizure. With a nonconvulsive status seizure,
there is a loss of consciousness or altered sensorium with min-
imal face or limb movement.
Infections of the Nervous System
A multitude of infectious etiologies affect the nervous system.
The two most common that are addressed in the neuroscience
ICU are bacterial meningitis and viral encephalitis. Both types
of infections can be extremely toxic, imposing life-threatening
complications to the acutely ill patient.
Bacterial Meningitis
Bacterial meningitis is a pyogenic, or purulent, infection that
involves the pia-arachnoid layers of the meninges, the sub-
arachnoid space, and the cerebral spinal fluid (CSF) (Hickey,
2003). This type of infection primarily occurs in one of three
ways: (1) bacteria gain access either via blood or through the
spread of nearby infections, such as sinusitis oritis; (2) CSF is
contaminated through surgical procedures or by penetration
 Common Neurologic Disorders and Evidence-Based Interventions 381

Box 28-3
Emergency Medical Management for Status Epilepticus
1. Standard ABCs of Life Support
• Support airway (most likely requires intubation)
• Maintain blood pressure
• Support circulation
2. Pharmacologic Management
• Recommended initial first-line therapy is a benzodiazepine; lorazepam (Ativan®) 0.1 mg/kg at  2 mg/min
• Act as agonists at GABAa receptors and promote inhibition of neuronal firing
If seizure activity persists
• Second-line therapy is hydantoins, phenytoin (Dilantin®) 20 mg/kg at  50 mg/min, fosphenytoin (Cerebyx®)
20 mg/kg at 150 mg/min
• Followed by scheduled daily dosing
If seizure activity persists
• Midazolam (Versed®) 0.1–0.3 mg/kg followed by continuous IV infusion of 0.05–2.0 mg/kg/hr
• Shown to rapidly control seizures that have not responded to traditional first- and second-line agents
If seizure activity persists
• Propofol (Diprivan®) initial dose 3–5 mg/kg followed by continuous IV infusion of 1–15 mg/kg/hr
If seizure activity persists
• Phenobarbital (Luminal®) 10–20 mg/kg at  50 mg/min or pentobarbital (Nembutal®) 5–12 mg/kg followed by
continuous infusion of 1–10 mg/kg/hr
• Goal of therapy is to achieve a comatose state with a “burst suppression” pattern on EEG
3. Once there is a cessation of seizure activity for over 12 to 24 hours, a slow taper of continuous IV infusions
should begin with the goal of treating complications and preventing recurrent seizure activity.
Sources: Bassin, Smith, & Bleck, 2002; Chapman, Smith, & Hirsch, 2001.

of invasive catheters that reside in the brain; or (3) bacteria
invade the meninges through the skull or other dural defects.
Community-acquired bacterial meningitis is typically caused
by such organisms as Streptococcus pneumoniae, Haemophilus
ylococcus influenzae, and Neisseria meningitides, whereas
hospital-acquired meningitis is usually caused by Staphylo-
coccus aureus, Streptococcus A and B, Escherichia coli, Klebsiella,
Proteus, and Pseudomonas. Both community- and hospital-
acquired meningitis produce similar classic signs and symp-
toms, including fever, headache, nuchal rigidity, altered level of
consciousness (LOC), and photophobia.
The gold standard for the diagnosis of meningitis is direct
CSF evaluation via lumbar puncture or aspiration of CSF from
ventricular tubing. Treatment measures should be immediate,
with initial interventions including general supportive treat-
ments for complications such as septic shock, seizures, and in-
creased ICP. Drug therapy should begin immediately, using
broad-spectrum antibiotic coverage until the causative organ-
ism is identified. In most cases, intravenous antibiotics are
warranted for many weeks to ensure complete irradication of
the infectious organism. Highly resistant organisms, such as
methicillin-resistant staphylococcus aureus, may require direct
antimicrobial contact through the intrathecal route in con-
junction with intravenous therapies.
Viral Encephalitis
Viral encephalitis is of sporadic or epidemic occurrence and
can be caused by a multitude of atypical viruses, including
herpes simplex virus, Epstein-Barr virus, and mosquito-trans-
mitted organisms (malaria, West Nile, Eastern equine, Western
equine, and St. Louis). The severity depends on the virus type.
Viral encephalitis can produce rapid deterioration in a pa-
tient’s neurologic status. Its many signs and symptoms vary
according to the invading organism and the area of the brain
involved (Hickey, 2003). Basic symptoms, such as fever,
headache, stiff neck, and change in LOC, are similar to those
exhibited with bacterial meningitis. More severe symptoms
progress to seizure activity, coma, and paralysis.
 382 CHAPTER 28 Common Neurologic Disorders
Viral encephalitis is diagnosed by serological and CSF
analysis, as well as through the patient’s clinical exam. There is
no definitive treatment for viral encephalitis and, in most cases,
a specific viral etiology is never identified. Supportive care
measures for secondary complications focus on the usual stan-
dard of care and can last weeks or months, depending on the
severity of symptoms and the rate of neurologic improvement
(Box 28-4).
Herpes simplex encephalitis type 1, which is associated
with the common cold sore, is a particularly severe form of
encephalitis with a very high morbidity and mortality rate.
Intravenous acyclovir (Zovirax®), given prior to the onset of
coma, is the standard of treatment.
Brain Death
Brain death is defined as a total loss of brain function, mean-
ing life has come to an end and the patient has passed away
(Wijdicks, 2003). Life support is futile, but is continued briefly
to make organ donation possible. Brain death in adults is fre-
quently a consequence of severe traumatic brain injury or of
compartment syndrome of the brain from a massive hemor-
rhage causing cerebral herniation. The task of declaring brain
death, which includes a precise clinical examination, interpre-
tation of diagnostic findings, ruling out conditions that mimic
brain death, and proper execution of brain death determina-
tion practices, is extremely complicated for the neuroscience
specialist. Complete destruction of the brainstem, where most
autonomic reflex function is controlled, is required to confirm
brain death. Box 28-5 describes the clinical criteria for deter-
mining brain death in adults.
Box 28-4
Common Supportive
Care Measures for Viral
Encephalitis
• Steroids to control malignant cerebral edema
• Mechanical ventilation for respiratory support
• Anticonvulsants/EEG monitoring for seizure
prevention
• Continuous or frequent analgesics for pain
control
• Sedatives for anxiety and to decrease cerebral
metabolic demand
• Antipyretics/endovascular cooling to control
hyperthermia
Box 28-5
Clinical Criteria for
Brain Death in Adults
• Coma—no eye opening to a painful stimulus
• Absence of motor response to a painful
stimulus
• Absence of pupillary response to light—
pupils midposition and dilated 4–6 mm (CNs
II, III)
• Absence of corneal reflexes—reflexive eyelid
closure with corneal stimulus (CNs V, VII)
• Absence of caloric response—reflexive eye
deviation toward cold stimulus injected di-
rectly into the inner ear (CNs VIII, III, VI)
• Absence of a gag and cough reflex in re-
sponse to deep suctioning (CNs IX, X)
• Positive apnea test—absence of a respira-
tory drive at a partial pressure of arterial car-
bon dioxide (PCO2) that is 60 mm Hg or 20
mm Hg above normal baseline values
The clinical examination and apnea testing are
generally performed by two separate physicians
6 hours apart although requirements vary per
institution.
Sources: Wijdicks, 2001; Wood, Becker, McCartney,
D’Alessandro, & Coursin, 2004.
In addition to the clinical exam, confirmatory diagnostic
testing may be used at the physician’s discretion, or if situations
such as hypothermia, sedation, or metabolic derangements
cloud the diagnosis of brain death. To document cessation of
blood flow through the cerebrovascular system, bedside test-
ing is preferred.
Once brain death is confirmed, organ procurement is an
option if vital functions are artificially maintained, the family
requests or agrees to donation, the patient fits donation crite-
ria, and the patient’s organs are not irreversibly damaged. The
Federal Conditions of Participation of the Centers for Medicare
and Medicaid Services require hospitals to notify their local
organ-procurement organization in a timely manner of im-
pending death. “Timely” means notification prior to brain
death or before the withdrawal of life support. Potential donors
must be ruled in or out based on exclusion criteria. Once a
potential donor is identified, discussions regarding donation
can be initiated with the family (Wood, Becker, McCartney,
 Case Study 383

D’Alessandro, & Coursin, 2004). Chapter 59 provides more
detail on organ donation.
PATIENT OUTCOMES
Nurses can help ensure attainment of optimal patient outcomes
such as those listed in Box 28-6 through the use of evidence-
based interventions.
SUMMARY
Being an ICU nurse in the care of a neurologically compro-
mised patient is challenging and requires high levels of clini-
cal judgment in the management of symptoms. Collaborative
care teams have shown to improve morbidity and mortality
in this critically ill population. The medical and nursing com-
munity can continue to improve this trend by practicing under
evidence-based guidelines and moving toward greater achieve-
ments in research through data collection and continuing ed-
ucation. Knowledgeable ICU nurses are extremely vital prac-
titioners to the team, striving to accomplish the primary goal
of quality, cost-efficiency, and compassionate care.
Box 28-6
Optimal Patient Outcomes
1. Intracranial pressure in expected range
2. Neurologic findings in expected range
3. Patient safety maintained during seizure
activity
4. Absence of signs and symptoms of infection
5. Family uses effective coping strategies
6. Patient/family expresses readiness for death

CASE STUDY
B.H. is a 36-year-old female who was brought into the emergency department with a history of being confused during the morn-
ing hours. Her confusion was apparent when she went to the bank and could not remember how to drive herself back home. She
stopped to ask for directions and ultimately asked someone to call her husband, who came to take her to the hospital. She com-
plained of having the “worst headache” of her life.

Physical Examination
The patient had a Glasgow Coma Scale score of 14, intact cranial nerves, headache with a score of 10 on a scale of 1 to 10, neck
stiffness, photophobia, and low back pain. Her blood pressure was 178/92 with heart rate of 88. The monitor displayed a normal
ECG. She was afebrile.

Diagnostic Tests
CT scan of the head revealed a small subarachnoid hemorrhage indicating a grade I SAH. The patient had a CT angiography and
then an intra-arterial digital subtraction angiography with three-dimensional imaging. A decision was made to proceed with mi-
crosurgical treatment. Microsurgical treatment involved clipping the aneurysm using nonmagnetic titanium clips.

Postoperative Management
The patient was monitored and treated for several days in the ICU by a team of nurses, physicians, and other healthcare profes-
sionals. The patient was transferred to a neuro stepdown unit for several days prior to being discharged to a rehabilitation unit.

CRITICAL THINKING QUESTIONS

1. What are three symptoms of cerebral aneurysm?

2. What are the components of triple-H therapy?
3. List five aneurysm precautions for the preoperative patient.
4. Design a teaching plan for the family of an SAH patient.
 384 CHAPTER 28 Common Neurologic Disorders

5. Use the form to write up data and a plan of care for a patient with SAH in the clinical setting. Rate the patient as a
level 1, 3, or 5 on each characteristic. Identify the level of nurse characteristics needed in the care of this patient.
6. Take one patient outcome for a patient and list evidence-based interventions found in a literature review for this
patient.

Using the Synergy Model to Develop a Plan of Care

Subjective and Evidence-based

Patient Characteristics Objective Data Interventions Outcomes

Resiliency

Vulnerability
SYNERGY MODEL

Stability

Complexity

Resource availability

Participation in care

Participation in
decision making

Predictability

Online Resources
American Stroke Association: www.strokeassociation.org/presenter.jhtml?identifier=1200037

National Stroke Association: http://nfo.stroke.org/site/PageServer?pagename=HOME

National Institute of Neurological Disorders and Stroke: www.ninds.nih.gov/

American Heart Association Stroke Guidelines: www.americanheart.org/presenter.jhtml?identifier=3004586

Stroke Coding Guide of the American Academy of Neurology: www.stroke-site.org/guidelines/stroke_coding.html

Epilepsy information: www.epilepsy.com/

Meningitis Research Foundation: www.meningitis.org/

The Brain Aneurysm Foundation: http://www.bafound.org/info/subarachnoid.php


REFERENCES
Adams, H. P., Brott, T. G., & Cromwell, R. M. (1994). Guidelines for the
management of patients with acute ischemic stroke: A statement for health-
care professionals from a special writing group of the Stroke Council, American
Heart Association. Stroke, 25, 1901–1914.
Ahmed, N., Nasman, P., & Wahlgren, N. G. (2000). Effect of intravenous
nimlodipine on blood pressure and outcome after acute stroke. Stroke, 31,
1250–1255.
Albanese, J., Leone, M., & Alliez, J. R. (2003). Decompressive craniectomy
for severe traumatic brain injury: Evaluation of the effects at one year. Critical
Care Medicine, 31, 2535–2538.
Bassin, S., Smith, T. L., & Bleck, T. P. (2002). Clinical review: Status epilep-
ticus. Critical Care, 6(2), 137–142.
Caplan, L. R. (2004). Thrombolysis 2004: The good, the bad, and the ugly.
Review of Neurological Disease, 1(1), 16–26.
Chapman, M. G., Smith, M., & Hirsch, N. P. (2001). Status epilepticus.
Anaesthesia, 56(7), 648–659.
Cho, D. Y., Chen, T. C., & Lee, H. C. (2003). Ultra-early decompressive
craniectomy for malignant middle cerebral artery infarction. Surgical Neu-
rology, 60, 227–232.
Commichau, C., Scarmeas, N., & Mayer, S. (2003). Risk factors for fever in
the neurologic intensive care unit. Neurology, 60(5), 837–841.
Durward, Q. J., Amacher, A. L., & DelMaestro, R. F. (1983). Cerebral and
cardiovascular responses to head elevation in patients with intracranial hyper-
tension. Journal of Neurosurgery, 59, 938–944.
Forster, N., & Engelhard, K. (2004). Managing elevated intracranial pres-
sure. Current Opinion in Anaesthesiology, 17(5), 371–376.
Hickey, J. V. (2003). The clinical practice of neurological and neurosurgical
nursing (5th ed.). Philadelphia: Lippincott Williams & Wilkins.
Josephson, L. (2004). Management of increased intracranial pressure.
Dimensions of Critical Care Nursing, 23(5), 194–207.
Juvela, S., Siironen, J., & Kuhmonen, J. (2005). Hyperglycemia, excess
weight, and history of hypertension as risk factors for poor outcome and cere-
bral infarction after aneurysmal subarachnoid hemorrhage. Journal of Neuro-
surgery, 102(6), 998–1003.
Liu-Deryke, X., & Rhoney, D. H. (2006). Cerebral vasospasm after aneurys-
mal subarachnoid hemorrhage: An overview of pharmacologic management.
Pharmacotherapy, 26(2), 182–203.
References 385
National Institute of Neurological Disorders and Stroke rt-PA Stroke Study
Group. (1995). Tissue plasminogen activator for acute ischemic stroke. New
England Journal of Medicine, 333, 1581–1587.
Ohkuma, H., Tsurutani, H., & Suzuki, S. (2001). Incidence and signifi-
cance of early aneurysmal rebleeding before neurosurgical or neurological
management. Stroke, 32(5), 1176–1180.
Paolino, A. S., & Garner, K. M. (2005). Effects of hyperglycemia on neu-
rologic outcome in stroke patients. Journal of Neuroscience Nursing, 37(3),
130–135.
Sen, J., & Albon, B. A. (2003). Triple-H therapy in the management of
aneurysmal subarachnoid haemorrhage. Lancet Neurolinquist, 2, 614–621.
Shiozaki, T., Nakajima, Y., Taneda, M., Tasaki, O., Inoue, Y., Ikegawa, H.,
et al. (2003). Efficacy of moderate hypothermia in patients with severe head
injury and intracranial hypertension refractory to mild hypothermia. Journal
of Neurosurgery, 99(1), 47–51.
Singh, V. (2004). Critical care assessment and management of acute is-
chemic stroke. Journal of Vascular and Interventional Radiology, 15(1, Part 2),
S21–S27.
Steiner, L. A., Balestreri, M., Johnston, A. J., Coles, J. P., Smielewski, P.,
Pickard, J. D., et al. (2005). Predicting the response of intracranial pressure to
moderate hyperventilation. Acta Neurochirurgica, 147(5), 477–483.
Suarez, J. I., Osama, O., Suri, M., Feen, E. S., Lynch, G., Hickman, J., et al.
(2004). Length of stay and mortality in neurocritically ill patients: Impact
of a specialized neurocritical care team. Critical Care Medicine, 32(11),
2311–2317.
Varelas, P. N., Conti, M. M., Spanaki, M. V., Potts, E., Bradford, D.,
Sunstrom, C., et al. (2004). The impact of a neurointensivist-led team on a
semiclosed neurosciences intensive care unit. Critical Care Medicine, 32(11),
2191–2198.
Wijdicks, E. F. (2003). The clinical practice of critical care neurology (2nd
ed.). New York: Oxford University Press.
Wijdicks, E. F. (2001). Current concepts: The diagnosis of brain death.
New England Journal of Medicine, 344(16), 1215–1221.
Wood, K. E., Becker, B. N., McCartney, J. G., D’Alessandro, A. M., &
Coursin, D. B. (2004). Current concepts: Care of the potential organ donor.
New England Journal of Medicine, 351(26), 2730–2739.